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Topic: Can a Christian support evolution? (Read 19229 times)

I posted this question here because there isn't a specific one for science. I would like to see a forum started on science here. That would be fantastic.

I think that there are certain elements of evolution that may be true. Natural selection is one. But I question macroevolution. I know that there is a lot of evidence to support the idea of humans and apes sharing a common ancestor, but that doesn't necessarily mean that the conclusion that humans and apes MUST have evolved from the same group is inescapable.

Minor changes like Darwin's finches and their beaks is one thing. Sure, I believe that happens. But people coming from other primates? I highly doubt this.

I agree. To an extent, evolution does happen. Over time, species do adapt to new environmental challenges.

But as far as if humans and monkeys shared a common ancestor, I really can't give an answer other than God's plan was fulfilled. If in our creation, he took a shortcut and caused us to evolve from primates, then that's fine by me. I'm here today, and God is the reason. The truth is that there is no surviving evidence from that time which has ever been found, so we will most likely never know.

A messageboard that gets right into this topic with rip-roaring debates between Christians and athiests over evolution is [link deleted]. Look under 'communities' for the New Age and Spirituality messageboard. There are tons of threads on this topic.

A few words need to be said about the "theory of evolution," which most people take to mean the proposition that organisms have evolved from common ancestors. In everyday speech, "theory" often means a hypothesis or even a mere speculation. But in science, "theory" means "a statement of what are held to be the general laws, principles, or causes of something known or observed." as the Oxford English Dictionary defines it. The theory of evolution is a body of interconnected statements about natural selection and the other processes that are thought to cause evolution, just as the atomic theory of chemistry and the Newtonian theory of mechanics are bodies of statements that describe causes of chemical and physical phenomena. In contrast, the statement that organisms have descended with modifications from common ancestors--the historical reality of evolution--is not a theory. It is a fact, as fully as the fact of the earth's revolution about the sun. Like the heliocentric solar system, evolution began as a hypothesis, and achieved "facthood" as the evidence in its favor became so strong that no knowledgeable and unbiased person could deny its reality. No biologist today would think of submitting a paper entitled "New evidence for evolution;" it simply has not been an issue for a century.

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As a man of science (mechanical engineer), I would also like to see a science sub-forum where some of the issues of science (evolution, age of the earth/universe, etc), could be discussed. It would need to be closely monitored though, as such discussions quickly become heated.

There are many self-described Christians who believe in evolution. I am not one of them. There is a way to reconcile science and Genesis without treating Genesis in an allegorical manner. As a Fundamentalist Christian, I believe the Bible should be taken literally, unless it is obvious it should be taken another way. I believe in the Ruin-Reconstruction Theory (aka Gap Theory) of interpreting Genesis 1:1-1:3. This makes sense to me.

As a man of science (mechanical engineer), I would also like to see a science sub-forum where some of the issues of science (evolution, age of the earth/universe, etc), could be discussed. It would need to be closely monitored though, as such discussions quickly become heated.

There are many self-described Christians who believe in evolution. I am not one of them. There is a way to reconcile science and Genesis without treating Genesis in an allegorical manner. As a Fundamentalist Christian, I believe the Bible should be taken literally, unless it is obvious it should be taken another way. I believe in the Ruin-Reconstruction Theory (aka Gap Theory) of interpreting Genesis 1:1-1:3. This makes sense to me.

I think is just a logically-foolish theory. If some Christians believe it and reconcile it with the fact that God created all living things. . . I'm not sure I'd say it says anything about their faith.

The reason it's an issue is because many in the church come out and say that you can't be a Christian and believe in any part of evolution. Then you have those in science saying the exact same thing, all because of how they interpret Genesis.

It reminds me of the time of Galileo. The church insisted that his findings were heretical to the teachings of the Bible. Although we scoff at this notion today, back then it almost cost the man his life.

For many, the realy problem lies with the age of the earth. Anyone who knows much about science can tell you that there are three different ways to verify the age of the universe as billions of years old. This means that if you can undermine a method such as carbon dating, there are other methods to come to the same conclusion from other areas of science.

I often struggled with this topic until I read "Genesis and the Big Bang" by Dr. Gerald Schroeder. He is both scientist and theologian. After all, to marry both fields one must have knowledge in both to make correlations. In the book he cited ancient rabbis who came to the conclusion that the earth was much older than 6 thousand years. They reasoned this merely from the Hebrew terms used to describe morning and evening which were translated as meaning "disorder" and "order" by the rabbis.

It is an interesting book for those interested in Old Earth Creationist views.

All that I know is that the majority of our origins is a mystery, yet some proclaim to have all the answers. In reality, we are just like Job. We don't know all the answers but are surrounded by those who would judge us and tell us they do know all the answers.

The reason it's an issue is because many in the church come out and say that you can't be a Christian and believe in any part of evolution. Then you have those in science saying the exact same thing, all because of how they interpret Genesis.

It reminds me of the time of Galileo. The church insisted that his findings were heretical to the teachings of the Bible. Although we scoff at this notion today, back then it almost cost the man his life.

For many, the realy problem lies with the age of the earth. Anyone who knows much about science can tell you that there are three different ways to verify the age of the universe as billions of years old. This means that if you can undermine a method such as carbon dating, there are other methods to come to the same conclusion from other areas of science.

I often struggled with this topic until I read "Genesis and the Big Bang" by Dr. Gerald Schroeder. He is both scientist and theologian. After all, to marry both fields one must have knowledge in both to make correlations. In the book he cited ancient rabbis who came to the conclusion that the earth was much older than 6 thousand years. They reasoned this merely from the Hebrew terms used to describe morning and evening which were translated as meaning "disorder" and "order" by the rabbis.

It is an interesting book for those interested in Old Earth Creationist views.

All that I know is that the majority of our origins is a mystery, yet some proclaim to have all the answers. In reality, we are just like Job. We don't know all the answers but are surrounded by those who would judge us and tell us they do know all the answers.

Last paragraph is so true. I grew up indoctrinated in creationist views. It's blasphemy to suggest anything else to my 80 year old pastor father. He even had a Creationist scientist visit the church to talk.

Dr. Francis Collins does not let his evolutionary beliefs stand in the way of his faith. Being open minded is such a fear for some. As an adult, I realize my faith is strong and I'm not afraid to consider new findings in any area. If aliens landed tomorrow, it would not shake my faith. Ha-it would only make me question how I understood it. It would just give me new insight to God's mind and ways. People get so defensive about things God didn't assign us to defend. I think the basis is fear, the way a toddler throws a tantrum if you try to take their pacifier or security blanket or panics when you turn the corner into the other room. I know God is God and all will be well, regardless of new discoveries

It really comes down to how you interpret the first chapter in Genesis. A lot of people believe that when it says day the Bible means 24 hours. If this is the case than evolution is impossible because it would take tons of years for the process to be complete.

On the other hand some regard the "day" in Genesis as more of a period of time - several thousand years possibly. If this is the case than there is certainly room for evolution to exist.

The next thought then is, what does it mean when it says that God created man? This could still be evolution. Buuuuuut what about woman? She was made from Adam's rib. This doesn't fit into the evolutionary scene as far as I can tell.

This is my first post as a new member here and the topic is of interest to me. I've just submitted an essay to the "Philosophical Review," called the "Effect for Cause, or What for Why Fallacy, A Critical Response to Richard Dawkins." In the essay I've quoted from Darwin's "Origin of Species" from the section where he explains the process of natural selection. The claim is put forth that natural selection acts as a causal agency.

Some scientists are now debating more causal agencies apart from natural selection, but my interest is with those who argue that natural selection should and can be treated as an effect that is itself in need of an explanation. What brought about this agency of natural selection? Conor Cunningham mentions this in his book "Darwin's Pious Idea." I've also quoted Cunningham in my essay and have had some email correspondence back and forth with him.

My essay argues that natural selection is an explanation of what happens in nature, it is not an explanation (except in a limited sense) of why what happens in nature, happens. It's the explanation of a process that takes place. It describes this process, but it does not go to the extent of explaining why all of this change that happens, happens. There is a critical difference between explaining something that has happened, and explaining why this something has happened. This explains the title for my essay. What Dawkins and many other scientists are doing, along with many philosophers, is that they are confounding the explanation of an effect for an explanation of a cause, or the explanation of a what for an explanation of a why.

In the essay I've also mentioned a field study in Davis California, around Telegraph Hill, where some researches studied a group of feral pigeons. Some of the pigeons studied were found to have a distinctive white patch at the base of their tail feathers. Researches found that these pigeons escape capture by their predators (Peregrine falcons) more often than pigeons without this marking. They are ten times less likely to be captured. The researches went so far as to clip these white feathers from some of those pigeons born with this adaptation, and transferred these onto pigeons without this adaptation. They found that the capture rate of these pigeons that were given these feathers declined ten fold while those pigeons deprived of these feathers increased ten fold.

In a book called "The Making of the Fittest" the author, Sean B. Carroll, cites this study and claims that it proves that these pigeons are evolving under natural selection.

My argument is that the field study is only an explanation of something that has happened in nature. It does not amount to an explanation of why this something has happened. Carroll is making a fallacious causal claim in other words.

In this instance, as in many others, the mistake that scientists are making is that they are confounding two different sorts of explanations. They are confounding an explanation of something that has happened with an explanation of why that something, has happened.

The same holds true for Darwin's explanation of the causal agency of natural selection. It's the explanation of something that has happened. It is not an explanation that helps us to understand why this something that has happened, has happened.

The philosophers David Hume, Immanuel Kant, and even earlier, the philosopher Socrates, pointed out the critical difference between explaining an effect and explaining a cause. Hume points the distinction out in his "Treatise Concerning Human Nature," Kant points out the same distinction in his "Critique of Pure Reason," and "Prolegomena to Any Future Metaphysics," and Plato has Socrates mentioning the same critical difference in the "Phaedo" of his "The Last Days of Socrates." Socrates dismissed the claim of Anaxagoras made in this same regard. Socrates explains that all Anaxagoras offers is an explanation of something that has happened. He does not offer us an explanation of why this something that has happened, has happened.

I cite all the relevant statements by all three in my essay.

As a Christian, I see no problem with accepting the fact that the Earth is 4.6 billion years old, or that a progressive emergence of change has swept over the Earth over this course of time. But evolutionary theory does not explain why this process of emergent change has taken place. This is where a vast majority of Christians seem lost. They, just as evolutionists, cannot seem to grasp the crucial critical difference between explaining an effect and explaining a cause, or explaining a what and explaining a why. But there is a crucial, critical difference whether they care to see it or not, or whether they are able to see it, or not.

I posted this question here because there isn't a specific one for science. I would like to see a forum started on science here. That would be fantastic.

I think that there are certain elements of evolution that may be true. Natural selection is one. But I question macroevolution. I know that there is a lot of evidence to support the idea of humans and apes sharing a common ancestor, but that doesn't necessarily mean that the conclusion that humans and apes MUST have evolved from the same group is inescapable.

Minor changes like Darwin's finches and their beaks is one thing. Sure, I believe that happens. But people coming from other primates? I highly doubt this.

What do you think?

SD...we need to clarify terminology.

Evolution has four different meanings which evolutionists speed-shift through in order to confuse the issue and eventually force one to concede that evolution (man from amoeba) is truth. First, ADAPTATION is NOT evolution...if we take the basic form of the definition of evolution (change), then yes, life and organisms do change, but this is not "microevolution," this is adaptation, and to call them one and the same is the first step in leading into TOEist's definition trap.

Adaptation is mediated by genetic mechanisms that God has already built into organisms at creation, and only await signalling into expression via environmental cues. This throws evolutionary nonsense out the window, and destroys evolutionary population genetics and other "what-if" explanations that are today taught in our schools as facts when they are nothing more than assumptions based upon unwarranted and illegitimate suppositions (The Assumptions Behind The Theory of Evolution, Authorhouse Publications).

A few words need to be said about the "theory of evolution," which most people take to mean the proposition that organisms have evolved from common ancestors. In everyday speech, "theory" often means a hypothesis or even a mere speculation. But in science, "theory" means "a statement of what are held to be the general laws, principles, or causes of something known or observed." as the Oxford English Dictionary defines it. The theory of evolution is a body of interconnected statements about natural selection and the other processes that are thought to cause evolution, just as the atomic theory of chemistry and the Newtonian theory of mechanics are bodies of statements that describe causes of chemical and physical phenomena. In contrast, the statement that organisms have descended with modifications from common ancestors--the historical reality of evolution--is not a theory. It is a fact, as fully as the fact of the earth's revolution about the sun. Like the heliocentric solar system, evolution began as a hypothesis, and achieved "facthood" as the evidence in its favor became so strong that no knowledgeable and unbiased person could deny its reality. No biologist today would think of submitting a paper entitled "New evidence for evolution;" it simply has not been an issue for a century.

The problem here with Victor is that he is an ardent believer in TOE, even though he has been shown the evidence...because he, like other evolutionists, choose to ignore all of the facts and choose to keep believing what he has been taught. Futuyma is dead wrong in his statement, and he is wrong because the facts (when not doctored by unwarranted and illegitimate assumptions) do not support his claim. When we take the facts of nature at face value, and do not add such unwarranted and illegitimate assumptions to them, they support special creation, not TOE.

Futuyma uses the same battle tactics as all his predesessors - bullying..."the evidence in its favor became so strong that no knowledgeable and unbiased person could deny its reality." At least he is not as bold and engrated as others, calling non-believers in TOE complete idiots, nevertheless, his statements which Victor copies here are demonstrated by pure natural facts, as being out in left field as far as reality goes.

Evolution attempts to stand on four legs, none of which can hold it up, singly or together. They are time, chance, mutations, and natural selection. Let’s look at them one at a time, but without spending too much time on any one of them.

Time: evolution demands an enormous amount of time, for it is claiming that all life we know on earth descended from a common ancestor. That common ancestor is usually identified as being some kind of one-celled organism. The earth is said to be about 4.5 billion years old – and right now, for the sake of this argument we are going to go with that idea in terms of orbital, regular years as you and I know them. The first single-celled organisms were not around until about 3.5 billion years ago. It took them, from what we read, about another billion years to become multi-celled organisms with cells that had differentiation. Let’s look at just that for a moment.

First, a definition. Generation time is the time it takes the adult of one type of organism to propagate and the progeny to mature enough to propagate themselves. A generation time for humans would be about thirteen years minimum, but we sure hope our kids wait longer than that! Apes are between ten and fifteen years. A lot of animals are about one year. Rodents are a matter of weeks or months.

The little E.coli bacteria is twenty minutes. That’s how we can get so sick so fast, by the way. Bacteria can replicate at an enormous speed. For the sake of the argument, and to give every possible advantage to evolution, let’s give our first single-celled organism a generation time of one hour. And maybe only during daylight hours. That’s approximately twelve generations in a day. That’s 4,380 generations in a year.

Multiply that by a billion years. That is 4,380,000,000,000 generations. If a fish were to change to an amphibian, and then to a mammal, and then to us, how many generations would that take? Now think of the generation times of the larger animals. Even if we averaged out generation times to one year for all, that means we would need over a thousand times the amount of years the evolutionists say the earth has been in existence to get even the simplest evolutionary changes made. But we only have 2.5 billion years to get it all done after the first multicelled organisms appeared. Evolution does not have enough time if you think about generation times instead of simply years.

Chance: Evolution depends on beneficial mutations being selected for in a breeding population and also building on one another to produce new forms and functions. We have not discussed mutations yet, but let’s presume we can get definitely beneficial mutations at this point. They have two hurdles to cross.

First, a beneficial mutation must be selected for. It helps a lot if this mutation, then, is dominant and not recessive. The only way a recessive mutation can exert its influence is when both parents have it, thus guaranteeing at least some of the progeny will also have it. This can and does happen, but for a mutation to be selected for, it does help if it is dominant. Then only one parent need have it. But that is a minor hurdle compared to what must happen next.

Most mutations are called ‘unexpressed,’ meaning they do not show any effect in the body of the organism – or at least anything we are aware of as yet! Mutations whose effect can be seen are called expressed mutations. Expressed mutations run, conservatively, a thousand to one deleterious to possibly beneficial. There is something else important to understand. The only mutations we can consider in this argument are called heritable mutations, or those which are passed down from parent to progeny. These mutations are carried, in humans for example, in the sperm and egg cells. We have a lot of other mutations in our bodies, but they aren’t passed down to our children.

Now, if, in any given population, there is one or more than one new negative heritable mutation in each generation, that population is on the way to extinction. There’s no way around that. It is called "error catastrophe."

So we have to have less than one negative mutation showing up per generation. This means you need over a thousand generations to get that beneficial mutation. Can’t you have more than one positive mutation show up in any generation or every few generations? There are, after all, probably thousands of animals in one gene pool. Yes, there are, but if you have two beneficial mutations show up in one generation, then what happened in terms of the multitude of negative mutations which complete the picture?

And despite the rarity of these beneficial mutations, one must build on another, and then on another, and so on to turn a fish into a frog. How many generations would it take for the several hundred, or thousand mutations necessary for this to happen? And what are the chances of that second mutation being just the right sort to not only be selected for but to be in the right place in the genetic package to build on to the first one?

Mathematically, the chances of it happening are zero. There is no chance at all that beneficial mutations could accumulate in any population in such a way. There is a lot more to this argument which absolutely destroys the concept of evolution, but that is enough to try to deal with at first.

So what about mutations? Mutations are little changes in the genes or other parts of the chromosomes. Mutations can happen in what appear to be spontaneous ways. That is just our way of saying, however, that we have not identified all the causes. We have identified some: radiation and some chemicals, for example. When something is known to cause a mutation, it is called a mutagent.

One of the favorite creation arguments against mutations doing anything beneficial is to say they decrease information. That is not a good argument unless you take the time to define ‘information.’ There are two distinct types: stochastic and meaningful. If I write “aa aba aa” that contains seven bits of information using the stochastic definition. If I add some ‘c’s so it becomes “aaa ccc baa aa,” then I have added information. But it means nothing. However, if I say “do hit me,” there are seven bits of stochastic information that carry meaning. So that is meaningful information. If I add three more bits: “do not hit me,” I have added exactly the same number of bits I did before, but I have changed the meaning entirely. So if you want to talk about mutations changing information, or deleting it, be prepared to define your terms carefully. The cell has to be able to understand the meaning in the mutation.

What we can say about mutations, though, is that all of them appear to decrease specificity. Consider a protein. Here is a rendition of one:

In a protein, chains of amino acids fold into specific shapes, according to which amino acids are used, the timing of the folding, the temperature involved, and some other variables. Each protein’s shape determines its use – how it locks on to other parts of the cell to do what it is supposed to do. When a mutation happens, the protein affected then folds a little bit less specifically. This usually means something cannot lock on to it effectively or it cannot lock on where it is supposed to. What a cell usually does with defective proteins is simply take them apart and use the amino acids all over again. However if the instructions regarding the building of that protein are where the mutation has occurred, then a defective protein will continue being the result.

It is this decrease in specificity which allows some bacteria, for example, to become antibiotic resistant. Bacteria can easily mutate back and forth in ‘hot spot’ areas. These mutations are “A/non-A” mutations. They simply go back and forth, not on and on and on into different new mutations. In any bacteria population, then, there will be a variety of ‘types’ – and some of them will have a less specific folding in the area where antibacterial agents are designed to lock on to in order to disable the bacterial. If the agents cannot lock on, the bacteria survives. This is how the ‘super bugs’ happen in hospitals which can make people so sick – all the normal bacteria have been wiped out and the super bugs are left to propagate. The mutations which made them ‘super’ have decreased the specificity of their protein folding and so the antibacterial agents are ineffective with them. What is interesting, though, is that when these ‘super bugs’ are put back into a wild population of bacteria of their own type, they are quickly wiped out. That is because, in reality, they are not as robust as the normal bacteria.

That is a long explanation, but that is what mutations do. They decrease specificity in one way or another, be it with proteins or something else.

So what would a beneficial mutation be? It would be something where a loss of specificity of one kind or another yielded some kind of benefit to the organism. For the bacteria, it means being anti-biotic resistant. Yet these are not as robust as the general population. In humans a famous example of a ‘benefical’ mutation is the one which provides resistance to malaria. This mutation is not as terrific as evolutionists want us to suppose, though, for not only is it recessive, but when both the mother and the father have it, their children are at high risk for sickle cell anemia, which is lethal. This lack of specificity in making the red blood cell does provide some malarial resistance. It also brings death to the children when both parents have this recessive gene.

Beneficial mutations, evolutionarily, are supposed to not only confer advantage, but be able to build upon one another to provide new form and function, so that first cell could, given enough mutations through enough years, become the fern, the hippopotamus, the butterfly. This is not what we see mutations do, however. It is far more along the lines of wishful thinking on the part of the evolutionists.

Natural selection: this is the ‘big gun’ of evolution. This is what the theory absolutely depends on. According to evolution ideas, natural selection is what happens when some part of any population is at a disadvantage when the population is under pressure and that disadvantaged section is either killed or simply not able to breed. This leaves the more advantages section of the population to continue. The evolutionary idea is that this then leads to a strongly adapted population which has also been helped along by various beneficial mutations which have been naturally selected through time.

Let’s take a look at what actually happens in natural selection – what we have seen happen. First of all, every population has a variety in its members. This will be easiest to see using mammals. Whether it is cats, dogs, horses, or whatever, we see quite a variety in any given population, whether wild or domestic. Let’s take a hypothetical population of wild horses in Asia. Some are a little shorter, some a little taller. Some a little more muscled, some a little less. Some a little smarter, some a little less. You get the idea. Now, let’s put this population under pressure. Some speedy predators have moved into the territory and the horses with the longer, faster legs are much more likely to survive, right? Sure. The horses that don’t survive so well are the ones with the shorter legs.

But the shorter legs are also the legs which are, biologically, usually a little thicker-boned. Those thick bones don’t break as easily as thinner, longer bones do. However, if enough of those shorter-legged horses are killed by our new predators, that particular horse population has just lost a little of their ability to produce the variation of short legged members. This is natural selection. It deletes. It does not add. Nor can mutations make up the difference. Even if there were some truly beneficial mutations available to this horse population, they could not build up fast enough to make up for the losses that happen with natural selection.

So what is the final, real result of natural selection? Endangered species. Species which are so specialized in the environment in which they live that they are unable to produce enough variety in their members to allow any portion of their population to survive outside of that specific ecological niche. You simply cannot keep deleting sections of a population due to natural selection and have a population remain robust, able to diversify. It is that precise genetic diversification which is reduced in natural selection.

We can see what happens on a much faster time scale when we consider breeding our domesticated animals. When we wanted Thoroughbred race horses, we bred OUT the shorter legs. When we wanted St. Bernard dogs, we bred OUT the smaller dogs with the lighter coats. No breeding program can invent something not present in the population being worked with. We can only breed away from the traits we don’t want. The result? The same, in its own way, as endangered species. The inbreeding in German shepherds, for example, leads to hip dysplasia. The inbreeding of Dalmations has led to a high incidence of deafness. In speeding up selection on a domestic basis, we have shown that deleting the ability to vary in a species produces some very undesirable results. So whether it is natural selection or breeding selection, we get individuals and populations which are not as robust and varied as the originals.

And this takes us straight back to the truth of Genesis 1. The truth of what we know in genetics points out that, first, older populations were more robust, with greater variation available to any group. Second, variation becomes limited through time due to natural selection. Thus, logically, variation potential must have been greatest in the earliest populations. Genesis says God created these original populations with the built-in instructions that all propagation was to be by kind. Think of kind along the lines of what we would call family or sub-family in our taxonomic system today: feline, canine, bovine, equine, etc. The fact that we can breed donkeys and zebras together, for example, is a strong indication that they were originally from a single parent population. But that is as far as we can go genetically. There is no known way for any feline to develop from a non-feline or to become a non-feline. God said “according to kind” and He meant it.

There is an interesting list which appeared in National Geographic of October 1999. On page 51 was the following list of problems associated with mutations in the human genome. If any evolutionist has some similar list of beneficial mutations, we would really appreciate knowing about it. Please keep in mind, as you read this list, that one of the evolutionary claims is that natural selection weeds out bad mutations….

The beginning was the best – before mutations, and when so much variety was built into each original population that diversification would be the norm. This is what the Bible tells us was the true origin of the species.

Some scientists are now debating more causal agencies apart from natural selection, but my interest is with those who argue that natural selection should and can be treated as an effect that is itself in need of an explanation. What brought about this agency of natural selection?

I studied natural selection for five years, in an effort to try and get a natural understanding of what Darwin and others were trying to convince us of...and the conclusion that I came to is that there is a natural selection, but it does not operate in the metaphysical way that evolutionists want it to.

As a word picture, if we take a 10 gallon fish tank complete with fish, rocks at the bottom, plastic water plants, filled with water, etc., natural selection is represented by the rocks at the bottom of the tank, and the water which surrounds everything in the tank represents chance.

Natural selection does NOT weed out the inferior within a population, it weeds out "whoever gets killed" and that's it...the antelope that is running from the lion, gets a speck of dust that is flying around the air from the chase into his eye, he can't see the hole that he steps into, snapping his leg in two...the next thing he knows, the fangs of the lion sink into his throat. Nothing to do with being weak, sickly, or inferior - and everything to do with chance.

The tiny krill floating through the ocean currents, inhaled by a whale as it passes this way...nothing to do with being weak, sickly, or inferior...just chance.

We could go on and on...and in every scenario, chance rules. But...you can't make an evolutionary theory of nature creating all living things around you according to natural chance, so we have to look at something else and assign to mother nature the metaphysical powers of culling and directing the evolution of organisms. Anyone with half a brain, that will sit down and read the explanations that TOEists try desperately to make natural selection sound like real science, and then ask the hard questions that TOE can't answer, will see the truth of it.

Evolutionary theory belongs in the trash can, because it is a cumulative, explanatory collection of lies promulgated by men who desired to be free of God. And if any true Christian is caught up in those lies, once the facts of science are shown to them outside of the unwarranted and illegitimate assumptions TOEists attach to them, I am sure they will change their minds.

Here is a paper I have on the subject of mutations, it was reviewed and approved by Dr. Berry Hall, who is quoted and referenced several times.

This is part I

Delineation of Current Terminology: Confusion of the Mutation IssueD. A. Schoch (2011)

ABSTRACT

WITHIN the last few decades, awareness has developed in the world of genetics having to do with the nature of genetic change. According to classical thought, DNA damaging events and mutations occur randomly throughout the genome of organisms purely by accident. However, a growing body of evidence demonstrates that some genetic change occurs in non-replication, non-random events. The literature gives evidence of two distinct categories of genetic change addressed by the single term “mutation.” These two categories consist of (1) replication-dependent, random chance genetic changes, and (2) non-random chance genetic adaptive change that originate as non-replication dependent changes. Logically, failure to distinguish between these two processes by separate terminology may have caused problems in understanding genetic systems. This paper aims to examine and make delineation between these two phenomena, so further research can proceed with improved knowledge and understanding of genomic processes, which require clear differentiation. Reasonable misunderstanding of many issues concerning heritability, variation, adaptation, and especially mutation, appear as potentially misleading factors without such demarcation. This has the potential of directly affecting cancer research, as well as other pertinent medical fields dealing with genetic diseases.

WHY do we observe some mutations arriving on the scene exactly when needed for the survival of organisms? If mutations do indeed exist as random, undirected events, why do some demonstrate initiation by genetic mechanisms of the organism? How can mutations exist as both random and non-random genetic events at the same time? Have we discovered a paradox in the nature of genetic change, or are we observing two different phenomena at work? This paper addresses the subject of genetic change. Current belief concerning the nature of mutations has them occurring as random genetic changes with respect to timing and placement within the genome (Elson et al. 2001; Clancy 2008; Hall 1990). In other words, they can hit the genome of an organism whenever and wherever chance might take opportunity. The many causes of mutation, while important depending upon the nature of the topic, are not discussed in this paper. However, it is acknowledged that mutagens can change nucleotides either before, or during, the copying of a gene and if correction enzymes do not catch and rectify these mistakes, the mutation can potentially effect the gene product, which can prospectively effect the health of the organism. The term “mutation,” as currently used, denotes the accidental, random chance (ARC) copy error events that take place (or solidified by the failure of correction mechanisms) either before or after genetic replication, and has become plastic to the point of including any and all genetic change. Today, most scientists in the disparate fields of biology hold to this definition. However, the latest data demonstrates this view to be in error and in need of revision. For the purpose of clarity, this paper holds the definition of the word “mutation” as strictly ARC replication-dependent errors. From review of the literature, it is a well attested to fact that some genetic change occurring in organisms are not due to ARC replication-dependent copy errors or DNA damaging events. In the papers on the subject, these genetic changes have been called “adaptive” mutations and “Cairnsian” mutations (in any event, they are still called “mutations”). For the purpose of clarity, it is suggested that these “adaptive” changes be called Variational Genetic Changes (VGC’s), which this paper will adopt throughout the remainder of the discussion. This acronym is suggested because, unlike ARC replication-dependent genetic changes, adaptational and variational genetic changes exist as non-ARC changes that originate from allelic material already defined within the organism’s genome. In short, these variation-dependent genetic changes, rather than replication-dependent genetic changes, are mediated by the organism’s genomic mechanisms. This paper argues that differential classification and terminology between these two phenomena needs adopting, particularly regarding the observation in the literature that both types of genetic changes have differing mechanisms of origin. This paper demonstrates that two entirely different phenomena exists and argues that the traditionally held view of the definition of mutation subsists in opposition to the evidence in the literature. Because the findings of the data, in which the literature reveals two discrete phenomena rather than only one, go against traditionally held views of the biological community, they have become the seeds of controversy.

DISCUSSION

Mutations (replication-dependent, ARC genetic changes), as noted earlier, have a variety of causes, both extra-cellular (such environmental agents as radiation, X-rays, gamma rays, and chemical mutagens) as well as intra-cellular (such as normal metabolic processes, methylation, replication errors, and free radical agents). These DNA damaging events fall into several categories, such as oxidation, thermal disruption, methylation, mismatched bases, deamination, depyrimidination, and depurination. These can all cause various types of accidental random changes, such as substitutions, insertions, deletions, inversions, duplications, translocations, frameshifts, transitions, transversions, CPD’s and PPS’s. All of these can lead to serious defects within the organism incurring them, if they are not arrested by the various repair mechanisms found within cells. Such repair mechanisms as nucleotide excision repair (NER), photoreactivation, base excision repair (BER), nonhomologous end joining (NHEJ), homologous recombination repair (HRR), proofreading enzymes, mismatch repair (MMR), microhomology-mediated end joining (MMEJ), translesion synthesis, DNA damage checkpoints, SOS response, and if necessary, apoptosis. An organism’s DNA remains in constant exposure to a variety of mutagens that threaten to damage it, therefore, mutations are a part of life. Once the damage occurs, if not repaired, it can lead to mutation. Mutations can lead to hundreds of genetic illnesses and diseases (such as SCA, cancers, and tumors) that seriously hamper the health and well-being of the organism affected, to the point of suffering a painful and early death. Damage to DNA can come from many different sources, both before or during, cellular replication. If correcting mechanisms do not rectify the damage before replication occurs, or immediately afterwards by cellular proofreading enzymes, then from that point forward, the damage will become a replication-dependent mutation. Once the mutation becomes established in the cell (if missed by these correction mechanisms), the cell will no longer recognize it as an error, it will now be considered “fixed” within the DNA. The term “mutation” has become extremely plastic in definition, and has the potential to produce major concern. The nature of mutations (ARC genetic change) is degenerative and has entropic effects (the inevitable and steady deterioration of physical systems) upon the genome, which I call “biotic entropy” (BE). The concept of entropy (as it has to do with different fields of biology) has been discussed several times in the literature in different contexts and applications (Barton and de Vladar 2009; Iwasa 1988; Xia et al. 2002). BE is accurately compared to the entropy (measurement of “noise” or degradation) in a system of information (Gray 2009), and DNA is indeed a system of information within the organism. Mutation (ARC, replication-dependent genetic change) introduces random “static” or “noise” in the information contained within the genome that, if not arrested by correction mechanisms, can result in catastrophic illnesses and diseases. However, BE is held at bay, normally, by the cellular repair mechanisms working for the survival of the cell, and ultimately, for the survival of the organism. Since the advent of genetics, we have discovered many things about the genome, even more so now that the Human Genome Project has been initiated and completed. We have learned that DNA is divided up into chromosomes, and further divided into genes. We have learned much concerning the genomic processes that take place through the ancient art of animal husbandry, where skillful hands of animal breeders can bring out and sculpt beautiful variations of animals and birds. We have learned about variations of genes (alleles) and even greater – we are learning about how the genome stores these variant alleles, unexpressed, for future need.

Genes in storage waiting for expression

Research is uncovering the mechanisms of adaptation and gene storage previously hidden. For example, what previously had been thought of as “junk” DNA has been discovered to code for certain RNA sequences, as well as other gene products (Crosio et al. 1996; Huang et al. 2005) in a very highly regulated mechanism of information storage. Most of these sections of DNA that were previously thought of as non-coding regions are introns. Preventing accidental expression of genes when they are not needed is one possible reason genes are broken up by introns, while introns themselves have been discovered to be coding sections in their own right. These are not cases of mutation because they are not DNA injuries or damages, nor are they sought out by repair mechanisms for correction, nor are they replication-dependent changes. On the contrary, they are mediated by genomic mechanisms and carried out with extreme precision and accuracy. It appears that introns themselves are a part of the genomic storage mechanisms that keep unexpressed alleles for future use as the organism may require. Genes, having formerly been viewed as linear strings of nucleotide bases found in only one place within the genome, have now been demonstrated to sometimes be scattered in pieces (in trans) throughout the chromosomes like data sets on a computer hard drive. The discovery that genes act like computer data sets that can be reunited with each other and activated for expression is giving scientists in genomic studies an entirely different feel for how the genome works from what has been previously believed. Such trans-mediated gene products have been identified in the Drosophila genes mdg4 (Labrador 2001; Dorn et al. 2001) and lola (Horiuchi et al. 2003), and in the C. elegans genes eri-6 and eri-7 (Fischer et al. 2008). It is reported that genes eri-6 and eri-7 produce separate pre-messenger RNA’s that are trans-spliced together to generate a functional mRNA, eri-6/7. One question brought out by this discovery is: will there be proteins found such as eri-6 and eri-7 that are functional in and of themselves, that are also functional when trans-spliced together into a third functional product? It seems this could be a very real possibility. The main concern for this paper, however, is that trans-spliced genes are being labeled as replication-dependent ARC mutations when they are put back together for expression. The question remains, why are they being called mutations when they are obviously directed by the organism’s genomic mechanisms. What’s more, it has been reported by Chung et al. (2007) that there are reading frames in mammalian genomes that are dual-coding. The authors go on to describe three examples of how human genes (GNAS1, XBP1, and INK4a) are dual-coded, so that there are actually two products coded for within one reading frame, or that reading frames overlap one another, producing two different products. Exactly how much of the human genome has dual-coding within reading frames of genes are unknown at this point in time, however these authors have identified forty so far. How many more mechanisms of allelic storage might be found by future research? Some of these storage mechanisms have been demonstrated to be mediated by recombination and genomic rearrangements (Foster 2000, 1998; Harris et al. 1996) after being broken apart, presumably to keep them safely inexpressible until needed. Such trans-mediated genes are then spliced together again for expression via recombination or rearrangement mechanisms. Bull et al. (2000) records that recombination-dependent stationary-phase genetic changes take place at multiple sites within the genome. Hall (1998) lists several mechanisms and pathways for these adaptational genetic changes, including base substitutions, frameshifts, excision of mobile elements, and insertion of mobile elements – all mediated by the organism’s genomic mechanisms. Schneider and Lenski (2004) identify insertion sequence (IS) elements mediated by genomic mechanisms that both inactivate genes as well reactivate them when IS elements are excised by those same mechanisms. Schneider et al. (2004) goes on to say that “IS elements are also recognized by the recombination machinery of the cell, leading to complex rearrangements.” IS elements have been demonstrated to be a factor contributing significantly to genetic variability. McKenzie et al. (2000) have identified such adaptive changes that are controlled by the SOS response system, as well as adaptive changes that require specific recombination proteins. These events are not ARC mutational changes, they are being specifically managed by specific genomic mechanisms under the control of genetic processes. These authors conclude their paper by stating that, “Understanding the regulation of all of the different adaptive or stationary-phase mutation mechanisms will illuminate when, how, and whether cells adjust their mutation rates and mechanisms, thereby inducing heritable changes, and presumably increasing their options for survival.” Since this paper was published, the answer to the mutation rate has been answered, and will be addressed shortly.

The literature is enamored with labeling adaptive genetic changes as “beneficial mutations,” but are they really mutations? VGC’s are beneficial to the organisms in which they occur for survival, but they are not due to replication-dependent ARC mutations. VGC’s have been researched and examined in rich detail (Foster and Cairns 1992; Williams and Foster 1994; Cairns 1998; Sletcha et al. 2002; to name a few).

The data shows three main differences between DNA damage/mutations and VGC’s, first of which is that VGC’s are specific and exact in time and place, while mutations are random chance DNA damaging events. All VGC’s are specific to the exact need of the organism at a specific time. Loewe (2008) reports “The statement that mutations are random is both profoundly true and profoundly untrue at the same time.” This statement was made viewing ARC mutations and VGC’s as one phenomena, yet making the basic random / non-random distinction between the two (as dealing with both time and placement of such genetic changes). Hall (1997) states that “The aspect of adaptive mutagenesis that remains the most contentious is the specificity of adaptive mutations,” while demonstrating that adaptive changes are specific to the “selective challenge(s)” bombarding organisms. In other words, the organism encounters an environmental challenge to survival and its genomic mechanisms meet that challenge by expressing previously stored variational alleles. Hall (1990) demonstrated that such VGC’s only occurred when they were needed by the cell incurring the change. In later experiments, Hall (1998) demonstrated again the difference between replication-dependent changes (mutations) and variation-dependent changes – which is again the specificity of time and place. Riesenfeld et al. (1997) reports that “adaptive mutations seem to produce only those phenotypes which allow the cells to grow, whereas growth-dependent mutations occur randomly with respect to their effects on fitness” demonstrating that adaptive changes are indeed specific to the needs of the cell. Cairns and Foster (1991) have demonstrated that VGC’s are produced according to the needs of the cell, unlike the nature of the occurrences of ARC mutational changes. Harris (1996) demonstrated that stress responses are initiated to generate the appropriate genetic changes in order to arrest that stress, again showing that VGC’s are directed for the adaptational survival of the cell. Cairns et al. (1988) performing experiments on E. coli, reported the bacteria must have some way of “producing” or “selectively retaining” specific genetic changes for the needs of the cell in order to survive, because the bacteria was producing the exact adaptive changes they needed in order to survive. These adaptive changes are possible because of the genetic variability stored within the chromosomes that can be signaled into expression by environmental stressor cues. The specificity of time and place of VGC’s are one reason they were first called “directed” mutations, and later as “adaptive” mutations in the papers examining them. When VGC’s were first identified in the literature, it was thought they represented extremely high mutation rates that would have fostered the right mutation for that specific circumstance. However, this hypothesis is no longer used to explain such adaptive changes (Foster 2000). It has been demonstrated experimentally on E. coli that such adaptive changes are not dependent upon increased mutation rates and, in fact, that there were no replication-dependent mutations – a rate of zero, so “no replication means no replication-dependent rate” (Hall 1990). Colby and Williams (1995) also corroborate Hall’s findings.

Second, the fact has been observed that VGC’s are mediated by different genomic mechanisms from those that are replication-dependent ARC mutations. Hall (1998) makes the observation that there are multiple mechanisms and pathways of VGC expression, and none of them are replication-dependent mechanisms which induce ARC genetic changes. Some of these adaptational changes are mediated by specific insertion sequence (IS) elements, via insertion and perfect excision of such mobile elements that turn “on” or “off” specific genes for expression (Schneider and Lenski 2004; Arjan et al. 2004), with over 500 such elements discovered so far. IS elements inactivate genes by means of reading frame disruptions (inserting themselves exactly where they are needed to do so), or reactivate said genes by reversions or the excisions of insertion activities previously mentioned. If it were not for the precision of IS element placements, they would be reeking havoc within the genome by turning on and off genes at random. Hall (1988) identifies IS elements as also providing promoters for specific genes as well as activating “cryptic” genes by inserting themselves into upstream regions of the chromosome. There is also evidence that some VGC’s are mediated by specific recombination events, making them recombination-dependent genetic changes, and further identifies specific enzymes implicated in initiating such recombination events by nicking (Foster 1998, 2000; Rosenberg et al. 1998). Foster states that recombination events rearrange “existing alleles” and can “create new ones.” Loewe (2008) further elucidates on this phenomena by stating these genetic processes can “lead to the production of new genes by pasting material from different genes together.” I submit that what’s being identified here, is previously inactivated genes through rearrangement processes, stored in-trans, being brought back together again for expression through recombination. Harris et al. (1996) further identify specific enzymes responsible for reading frame disruptions, which initiate recombination-dependent VGC’s. More enzyme-mediated VGC’s have been identified, such as Rpos-dependent events for specific gene expression (Lombardo et al. 2003). McKenzie et al. (2000) ratify that VGC’s are “tightly regulated” responses by genomic mechanisms, not replication-dependent ARC mutational events.

Third, it has been observed that VGC’s are variation-dependent, non-ARC genetic changes, while mutations are the exact opposite (Riesenfeld et al. 1997). Cairns et al. (1988) also identify VGC’s as being a property of cells in stationary phase, rather than being growth-dependent, which Hall (1997, 1998) confirms. VGC’s have been demonstrated to occur when chromosomes are not being actively replicated in E. coli during nutrition starvation (Williams and Foster 2007). VGC’s are not replication-dependent changes, but have been demonstrated to be stress induced, usually by environmental stressor elements. Another key difference between these two phenomena is that the cell has a variety of damage repair mechanisms in place to deal with the different kinds of damage that it suffers. In comparison, there are no known attempts by the cell to search out or repair VGC’s – indicating that cells do not recognize them as “damages.” In fact, they are not DNA damage, nor mutations. On the contrary, they are part of normal genomic processes for the continued survival of the organism via adaptation. These discoveries explain the phenomena observed in such cases as E. coli adaptation (Cairns et al. 1988) where the authors make the statement, “bacteria apparently have an extensive armoury of such ‘cryptic’ genes that can be called upon for the metabolism of unusual substrates.” Genes do indeed seem not only to be encrypted, but also broken up and dispersed throughout the genome to be called upon when needed. In every case, the needs of the organism appear to be environmentally induced.

Response to environmental cues

VGC’s in gene expression are induced specifically by the organism’s genome in response to environmental cues for the benefit of the organism. While ARC mutations can also be induced by environmental mutagens, they have the opposite affect. These environmentally cued genetic mechanisms give the organism access to varying phenotypes for survival and adaptability. How genetic mechanisms of adaptation and fitness relate to variation, working in connection with environmental cues, is a long standing question due to the lack of empirical studies documenting the causal relationships between the environment and the molecular underpinnings of fitness related variation (Storz 2007). Storz et al. goes on to identify the “difficulty of integrating molecular data with evidence for causal effects on organismal fitness” and examines specific mechanisms that enable organisms to adapt to their specific environments. These environmental cueing factors can be altitude (high or low), light cycles or light sensitivity (such as in deep sea dwelling organisms), temperature, diet (such as differing sizes and hardness of seeds impacting the thickness of bird beaks), humidity, hardness of soil, oxygen levels…any number of environmental dynamics (Ralson and Shaw 2008). All of these factors have an effect upon the organism’s phenotype, demonstrating a rich and complex interaction between genes and the environment (Lobo 2008; Lobo and Shaw 2008). These environmentally induced changes in gene expression are called “gene-environment interchangeability” and help the organism to adapt its phenotype to the specific “selective circumstances” they may find themselves in (Leimar 2009). The expression of the needed allele appears to be stress induced, caused by changes in the organism’s environment, which is why such changes are specific to the needs of the organism for its survival. These traits have been demonstrated by thousands of years of domestic breeding in hundreds of different species, such as bovine, dog, pigeon, etc. The only difference between domestic breeds and wild types is man’s hand culling and bringing out the traits he desires in each specific breed. We create more colorful birds, more milk producing cows, different dog breeds for work or for show, through careful breeding tactics. While, in the wild, these different allelic traits are only expressed in time of stress induced by the animal’s environment – but the genetic mechanisms are the same that operate in both cases. In some cases there are multiple environmental cues that signal genomic changes, such as both photoperiod and ambient temperature affecting the thermogenesis of the Djungarian hamsters (Heldmaier et al. 1982). In their study on domesticated cattle in Europe and Africa, Gautier et al. (2007) concluded from their research and observations that the genetic changes responsible for the variation between each population were not consistent with models considering replication-dependent ARC changes. To use a famous example, in “Darwin’s finches,” what are the environmental cues for the differences in beak size and thickness for each variation of bird on each different island? Presumably, the only cue seems to be the hardness of the seeds on which each island variety has to deal with. If this is true, is the exact environmental cue (for example) how many times a bird has to peck at the outer shell of the seed? Are the vibrations upon the beak from being hit against the hard shell some kind of trigger for beak thickness (in the same way that shivering thermogenesis is activated by the shivering of the body)? The speed of which these changes occurred in the finches is simply too fast to be considered strictly replication-dependent ARC mutations, they are more likely VGC changes activated into expression by the individual environmental cues the finches’ genome’s received after being first introduced to the islands. VGC’s are the exact opposite in nature as to their effects when compared with those of ARC mutations. Variational changes are beneficial genetic changes occurring within organisms, the materials of adaptation, while the effects of ARC mutations are nearly always deleterious to the organism. Two different phenomena, with different origins and with different final effects that are opposite one another. These facts seem to make clear that there is a natural distinction between these two genetic phenomena, one that we also need to differentiate between.

Conclusion

It all began with a paper by Cairns et al. (1988) that challenged the currently held view of mutations, and other papers quickly followed presenting concordant observations (Foster 2000). Such papers as these were viewed with much skepticism because they challenged the fundamental premise that all genetic change occurs only randomly as chance events without respect to any advantages they may give an organism (Colby and Williams 1995). Drake stated in her book, The Molecular Basis of Mutation (1970) that “It is clear that the experimental evidence supporting many currently popular hypotheses concerning mutational processes is quite inadequate.” Those words, written almost forty years ago, still appear to hold true today. Nevertheless, clarifying the terminology can advance understanding of biological processes. Addressing these different classes of genetic change, Hall (1990) stated, “although the two classes of mutations are basically distinct and have different molecular mechanisms…evidence for Cairnsian mutations has now been found in all cases where it has been sought.” According to the evidence in the literature, it appears that we are, indeed, observing two distinct classes of genetic change that must be differentiated between. If not, we could be inundated with perplexity in certain aspects of our research until these distinctions are recognized. For example, Hall himself (1988) illustrates this point in the following quote: “[W]e are ignorant of the fundamental mechanisms and rates of mutations in non-growing but metabolizing cells.” If we are talking about two entirely different phenomena, the mutations Hall addresses here are non-ARC genetic changes (VGC’s), in which there wouldn’t be a mutation rate because these changes occur naturally in populations only when they are cued by the environment. It is important for research to delineate between these two phenomena, for correct “characterization of individual beneficial mutations may lead to the identification of underlying molecular rules and constraints, as well as common adaptive pathways” (Rainey 2000; Travisano 2001; Otto 2002 as reported on by Arjan et al. 2004). The history of medicine demonstrates a succession of theories of disease and treatment. A strong evidence base is now a requirement for the adoption of new treatments. Similar criteria regarding strength of evidence should be applied to molecular science that now underpins many medical advances. The specificity of non-ARC genetic changes have been demonstrated experimentally (Hall 1997) numerous times by different scientists. Indeed, understanding the differential mechanisms of change, fully and correctly, is critical to the understanding of any genetic phenomena under investigation. Clarity about the origins, mechanisms, and results of both mutations (replication-dependent ARC genetic changes) and VGC’s (non-ARC genetic changes) will improve the quality of biological understanding. Colby and Williams (1995) make the statement, “taking these kinds of mutants into account may therefore be necessary to produce more accurate models of bacterial genome evolution.” Clearly, we are observing two different categories of events. These differences require terminology fit to distinguish the processes taking place. This would also distinguish between the mechanisms and results of each kind of change. And finally, Hall (1990) states, “Because the randomness of spontaneous mutations forms such a basic part of our view of biological processes, most of us may be more comfortable with an underlying random mechanism than with a directed one. We should be cautious, however, about rejecting the notion of ‘directed’ mutations simply because it makes us more comfortable to do so,” (Hall 1990). This is especially true when considering that these “directed mutations” do not appear to be random mutations at all, having their origins firmly grounded in completely different genetic mechanisms.

The problem here with Victor is that he is an ardent believer in TOE, even though he has been shown the evidence...because he, like other evolutionists, choose to ignore all of the facts and choose to keep believing what he has been taught.

Actually, I am ardent believer in the truth, if that leads me away from the TOE so be it. But for now, to me it is the best explanation of the current conditions of life on Earth.

10. Beyond a shadow of doubt, human DNA and chimpanzee DNA are 98% identical. We diverged from the same common ancestor 5 million years ago. This isn’t idle speculation, it is a fact bound up in deductive logic. We are the modern descendants of ancient apes, just as modern apes are the descendants from that same ancestral tree but on a different branch to humans. Just as the VW Beetle is the ancestor of the Porsche Carrera GT, one does not cease to exist because of the emergence of the other. But where car designs are engineered and refined by man, life is shaped by genetic mutations, which over time, gives rise to entirely new species.

9. The genetic evidence of natural selection is compelling enough proof of evolution without any evidence from fossils whatsoever. If Darwin had never lived, we would still have eventually discovered naturally occurring selection mechanisms in our DNA. If there were no fossils in the fossil record, whatsoever, the evidence of evolution in our genes would still be a fact. Genetics does not require the evidence from the fossil record in any way shape or form. Lateral gene transfer is a major mechanism in prokaryotic genome evolution. Gene theory and palaeontology are two completely separate areas of study that just so happen to support each other. Independently acquired, mutually corroborative evidence is the heart and soul of the theory of evolution. To disprove one, you must disprove the other, yet each set of evidences are intrinsically linked, while being independently ascertained.

8. Evolution does not propose origins of life. Evolution does not seek to answer the question of how the first multicellular organisms appeared. It describes how they evolved once they formed, not how they formed in the first place. Abiogenesis is in no way related to Darwinian evolution. We do not know how the first multicellular life formed, but we know what it was made of and that these elements were abundant on the early Earth, after it formed 4.54 billion years ago*, and that these same elements are present throughout the universe today. The vast timescales involved aren’t easy to comprehend. But admitting you do not understand something, in science, is the only way to find out.

Victor, check generation times against the fossil record and the claimed age of the earth and see if you still are willing to say evolution happened.

And then please be aware that EVERY mutation known (except for hot spot mutations which simply have 'on/off' features) involve a decrease in specificity. And then please explain how millions of decreases in specificity can get from a bacteria to a butterfly or a pine tree, or you.

Victor, check generation times against the fossil record and the claimed age of the earth and see if you still are willing to say evolution happened.

And then please be aware that EVERY mutation known (except for hot spot mutations which simply have 'on/off' features) involve a decrease in specificity. And then please explain how millions of decreases in specificity can get from a bacteria to a butterfly or a pine tree, or you.

One of the most common problems that laypeople have with evolution is that there doesn’t seem to have been enough time for it. Given the idea that evolution is relatively slow, and yet there’s been an enormous amount of change since the first species a few billion years ago, how could natural selection (and other processes like genetic drift) have built all these exquisite, functioning organisms?

Part of the answer, of course, is that people fail to appreciate “deep time,” since we’re evolved to regard life over years and decades, not millions and billions of years. Evolutionists often demonstrate this by compressing all of evolution into a calendar year, showing how much evolution has occurred in a short segment of that time. Using this analogy in WEIT, for example, I show that the divergence between the ancestors of humans and chimps would have occurred only at 6 a.m. on December 31.

Another difficulty is that people assume that if one species evolves into another by changing many traits, it seems highly unlikely that they can all change at the same time by simultaneous fixation of adaptive mutations. If evolutionary change of a species involves gene substitution at L genes (with L being a number), and the proportion of all genes in each generation that are more favored than the “primitive” type is 1/K (this number is low because most mutations are deleterious), then the number of “trials” it takes to get adaptive mutations at all the genes is on the order of KL . In other words, each generation new mutations arise, and if adaptive ones aren’t there for every gene required to make a descendant from an ancestor, then that whole trial is discarded and the process starts the next generation. Finally, after about KL generations have passed, you’ll get the right type.

Victor, you didn't pay any attention to my question. A generation time is the time it takes for an adult of any species to produce another adult of that species. For E.coli it is about 20 minutes. For apes it is about 10-12 years.

Here is a repeat of what I posted earlier:"Time: evolution demands an enormous amount of time, for it is claiming that all life we know on earth descended from a common ancestor. That common ancestor is usually identified as being some kind of one-celled organism. The earth is said to be about 4.5 billion years old – and right now, for the sake of this argument we are going to go with that idea in terms of orbital, regular years as you and I know them. The first single-celled organisms were not around until about 3.5 billion years ago. It took them, from what we read, about another billion years to become multi-celled organisms with cells that had differentiation. Let’s look at just that for a moment.

First, a definition. Generation time is the time it takes the adult of one type of organism to propagate and the progeny to mature enough to propagate themselves. A generation time for humans would be about thirteen years minimum, but we sure hope our kids wait longer than that! Apes are between ten and fifteen years. A lot of animals are about one year. Rodents are a matter of weeks or months.

The little E.coli bacteria is twenty minutes. That’s how we can get so sick so fast, by the way. Bacteria can replicate at an enormous speed. For the sake of the argument, and to give every possible advantage to evolution, let’s give our first single-celled organism a generation time of one hour. And maybe only during daylight hours. That’s approximately twelve generations in a day. That’s 4,380 generations in a year.

Multiply that by a billion years. That is 4,380,000,000,000 generations. If a fish were to change to an amphibian, and then to a mammal, and then to us, how many generations would that take? Now think of the generation times of the larger animals. Even if we averaged out generation times to one year for all, that means we would need over a thousand times the amount of years the evolutionists say the earth has been in existence to get even the simplest evolutionary changes made. But we only have 2.5 billion years to get it all done after the first multicelled organisms appeared. Evolution does not have enough time if you think about generation times instead of simply years."

An interesting comment, by the way, was made by Henry Gee (chief science writer for Nature at the time he wrote the book this comes from) regarding Deep Time:

"Deep Time is like an endless, dark corridor, with no landmarks to give it scale. ...A fossil can be though of as an event in Deep Time. Compared with the immensity of time in which it is found, a fossil is a point in time of zero extent: a fossil either exists or it doesn't. By itself, a fossil is a punctuation mark, an interjection, an exclamation, even, but it is not a word, or even a sentence, let alone a whole story...You cannot connect one fossil with any other to form a narrative....In the end, we never see fossils as they are, but only imperfectly, in the light of models that are more or less approximate. Given this constraint, it is surely hard enough to make progress understanding the evidence we have without leaping way beyond it, with presuppositions about chains of ancestry and descent, and about missing links. Such presuppositions are exposed as vacuous once the evidence finally catches up." (Henry Gee, In Search of Deep Time; The Free Press, 1999, pp 26-27, 85)

Henry Gee spends the rest of the book trying to get around this via cladistics.

Victor, you didn't pay any attention to my question. A generation time is the time it takes for an adult of any species to produce another adult of that species. For E.coli it is about 20 minutes. For apes it is about 10-12 years.

Did you read the article I posted?

There’s plenty of time for evolution...But that can take a huge amount of time. If you want to change 20,000 genes, for example, with only 1/40 of all segregating mutational variants being advantageous, then it would take 1034,040 “trials” (roughly the time it takes for a new adaptive mutation to become fixed) to effect this change. This could never occur, since even with an organism having 100 generations per year and with a “trial” equivalent to one generation, this would take a number of years equal to 10 followed by 34,038 zeroes. (Since life began there’s only been about 3 followed by nine zeroes years.) That’s not long enough!

As you’ve probably already guessed, evolution doesn’t work this way. As evolutionary change is occurring at one gene, it’s simultaneously occurring at other genes, affecting other traits, if there are adaptive mutations in the populations for those traits too. A “trial” doesn’t involve producing variants at every gene, with evolution occurring only if all of the genes have adaptive variants. Rather, in each trial the new adaptive mutations arise and begin their march toward fixation in some genes, leaving the rest to change during subsequent trials. In other words, evolution occurs in parallel rather than in series.

How does that change the speed of evolution? This is the topic of a new paper in PNAS by Herbert Wilf and Warren Ewens, a paper with the endearing title given above, “There’s plenty of time for evolution.” (I don’t know of another scientific paper whose title contains a contraction.) The point of Wilf and Ewens’s paper is to show mathematically that simultaneous substitution is much much faster than “serial” substitution, so that substantial evolutionary change can take place relatively quickly. This isn’t a new point, but the equations are new, and they show, as the title says, that there has been plenty of time for lots of evolution to have taken place.

If that were true, it would not have taken the supposed billion years to get from bacteria to multicellular organisms. In addition, would you please show me one KNOWN mutation which is a) not a hot spot mutation and b) also not one which decreases specificity? Thank you.

If that were true, it would not have taken the supposed billion years to get from bacteria to multicellular organisms. In addition, would you please show me one KNOWN mutation which is a) not a hot spot mutation and b) also not one which decreases specificity? Thank you.

LET US CONSIDER a frequent claim of creationists — that evolution is false because it requires a sequence of beneficial mutations, which are impossible. To find an example of an argument like that, we went to Answers In Genesis, and we weren’t disappointed. They have this essay: Are mutations part of the “engine” of evolution? Excerpt:

For molecules-to-man evolution to happen, there needs to be a gain in new information within the organism’s genetic material. For instance, for a single-celled organism, such as an ameba, to evolve into something like a cow, new information (not random base pairs, but complex and ordered DNA) would need to develop over time that would code for ears, lungs, brain, legs, etc.

Here’s the article’s conclusion:

The biblical perspective on change within living things doesn’t require that new information be added to the genome as pond-scum-to-people evolution does. In fact, we expect to see the opposite (loss of genetic information) due to the Curse in Genesis 3. Biblically, we would expect mutations to produce defects in the genome and would not expect mutations to be adding much, if any, new information.

Observations confirm that mutations overwhelmingly cause a loss of information, not a net gain, as evolution requires.

Okay, what’s the response? One clear example should suffice, so let’s make it a good one. Ideally, it should be something newly-evolved that wasn’t carried aboard Noah’s Ark. Can we find such a mutation? Yes, we have one. This is probably the most impressive example of all — Nylon-eating bacteria (bold added for emphasis):

In 1975 a team of Japanese scientists discovered a strain of Flavobacterium living in ponds containing waste water from a factory producing nylon that was capable of digesting certain byproducts of nylon 6 manufacture, such as the linear dimer of 6-aminohexanoate, even though those substances are not known to have existed before the invention of nylon in 1935.

Further study revealed that the three enzymes the bacteria were using to digest the byproducts were novel, significantly different from any other enzymes produced by other Flavobacterium strains (or any other bacteria for that matter), and not effective on any material other than the manmade nylon byproducts.

Creationists often say that all mutations are harmful and deleterious, and degrade the genome. They say that mutations can only scramble the information that's there, and that mutations cannot produce new "information." This page shows why they are wrong.

Last Update: November 5, 2004

My favorite example of a mutation producing new information involves a Japanese bacterium that suffered a frame shift mutation that just happened to allow it to metabolize nylon waste. The new enzymes are very inefficient (having only 2% of the efficiency of the regular enzymes), but do afford the bacteria a whole new ecological niche. They don't work at all on the bacterium's original food - carbohydrates. And this type of mutation has even happened more than once!

One central issue in the debate over Darwinian evolution is the question of evolutionary novelty -- can evolution produce truly novel features? The consensus of modern scientific research is that mutation and natural selection together can indeed produce novel, beneficial features in biological systems. Scientists further postulate that this low-level novelty extends to entire populations, which can, over time, become entirely separate species.

On the other hand, creationist and intelligent design writers have insisted that whereas minor changes may occur within an established "kind," nothing fundamentally new can come through "random" or "undirected" evolution. In any event, so they argue, no significant changes have ever been observed in biological species, so that evolution must be regarded only as a "theory" [Dembski2002].

Specific examples of evolutionary novelty

But numerous instances of evolution in action have been observed in the natural world, often generating novel, beneficial features within just a few years or decades. Here are just a few examples:

1 1974 E. coli experiment. In a 1974 paper Barry Hall and Daniel Hartl identified a gene in the bacterium E. coli that is responsible for metabolizing lactose, using a complicated three-part process. They removed this gene, and then permitted the bacteria to multiply in a stressed environment containing lactose. Within 24 hours the bacteria had evolved a capability to utilize lactose, by means of a similar but distinct three-part biochemical pathway, involving two mutated genes [Hall1974; Miller1999, pg. 145-147]. Biologist Douglas Futumya described this discovery as follows: "One could not wish for a better demonstration of the neo-Darwinian principle that mutation and natural selection in concert are the source of complex adaptations." [Futumya1986]. Biologist Kenneth Miller points out that not only is it a valid example of evolutionary novelty, it is also an example of a multi-part biochemical system that intelligent design writer Michael Behe has insisted could not be produced by natural evolution [Miller2005]. See also the discussion of Complexity.

2 1994 E. coli experiment. In a more recent experiment, biologist Richard Lenski and his colleagues conducted a 20-year experiment, starting with 12 flasks of E. coli bacteria, identical except for some neutral markers, and then each day inserting 1/100 of the flask's liquid (which contained glucose and citrate, among other materials) into a new flask. In this way they followed the course of these bacteria for 45,000 generations. As the generations continued, each of the 12 lines grew progressively better at processing glucose, although each took a different trajectory. Examining the results after 20,000 generations, the experimenters found that for two of the 12 lines, 59 genes had changed their levels of expression, and that all 59 had changed in the same direction in each line -- in other words, the two lines had independently "discovered" virtually the same improved scheme for glucose metabolism. Later in the experiment, shortly after generation 33,000, the average population of one of the lines shot up by a factor of six above the others. The investigators found that this line had developed the ability to utilize citrate, which bacteria normally cannot use, by means of a remarkable combination of two distinct mutations [Lenski1994; Dawkins2009, pg. 116-132].

3 2012 virus/E. coli experiment. In an experimental result announced in January 2012, a research team led by Richard Lenski demonstrated how colonies of viruses were able to evolve a new trait in as little as 15 days. The researchers studied a virus, known as "lambda," which infects only the bacterium E. coli. They engineered a strain of E. coli that had almost none of the molecules that this virus normally attaches to, then released them into the virus colony. In 24 of 96 separate experimental lines, the viruses evolved a strain that enabled them able to attach to E. coli, using a new molecule (a channel in E. coli known as "OmpF") that they had never before been observed to utilize. All of the successful runs utilized essentially the same set of four distinct mutations. Justin Meyer, a member of the research team, estimated that the chance of all four mutations arising "at random" is roughly one in 1027 (one thousand trillion trillion). Yet these lambda viruses acquired all four mutations in a matter of weeks [Zimmer2012].

4 Japanese nylon-eating bacteria. Japanese biologists recently discovered a bacterial species that thrives in nylon waste. It turns out that these bacteria had undergone a "frame shift" mutation, where an extra base pair had been inserted into the bacteria's DNA. This mutation significantly changed the bacteria's biology, since a long series of amino acids were altered, but by remarkable chance this alteration endowed the bacteria with the facility to metabolize nylon, albeit not very efficiently [Negoro1994].

Nylon-eating bacteria have suffered a decrease in specificity in the folding of their proteins. That is not what you are looking for, for one kind to change into another.

Second, the E.coli never became non-E.coli. In addition, 'they engineered' certainly indicated intelligent design, don't you think? I would also be curious if these were what is known as 'hot spot' mutations which simply operate like 'on/off' switches and occur rapidly in various sequences. They are never able, however, to go beyond turning on or off. It's A or B, never on to C or D, etc.

Let me know if they ever get something which is identified as a 'not E.coli' bacteria. Until that happens, and it is not a matter of degeneration, all the experiments (under very controlled circumstances you will notice) only show the remarkable ability to VARY within a species which God put into the kinds. Please also look into 'hot spot' mutations so you will see more how bacteria are able to do this sort of thing. It is how they survive in different environments. In sexual replication, gene mixing is able to produce the variations necessary. Bacteria reproduce asexually which means, if they did not have the ability to vary quickly within their type, they would have been extinct a long, long time ago.

Creationists oppose the idea that species can evolve indefinitely and charge evolutionary biologists with failing to define their terms properly. In this article I want to trace briefly the history of the idea of species and show that it is in fact a virtue of biology that it tries to make its terms follow the evidence rather than to define them all up front. The idea that species were universally thought to be fixed prior to Darwin is simply wrong — many creationist thinkers of the classical period through to the 19th century thought that species could change. The issue of evolution was, in fact, impossible to suggest until the claim was made that species were fixed, and as soon as it was suggested, so too was evolution. There has been a longstanding vagueness about living "kinds" that goes back to the classical era and that follows from good observation. What is more, nothing in the biblical or theological traditions requires that species are fixed, only that kinds exist, which neither evolutionists nor traditional creationists ever denied.

Because the number of species "concepts" in the literature is high, I have also tried to put them into context and list them for easy reference (see this page). That way, when a "concept" is referred to in a text, it can be compared to other candidate conceptions. It is clear to me, at any rate, that there are many conceptions of species, and that biologists use the one that best suits the organisms they study. I think of this as a "conceptual delicatessen" — when scientists need a species concept to suit the organisms being studied, they will typically assemble a custom "club sandwich" from previous ideas. This is not bad practice — if science is about learning and using words to express that learning, then we should expect that they would do this, and in fact they should.

To understand the concept of species, we must understand how the notion developed in the history of biological research. One point that must always be borne in mind: people did not suddenly become smart upon the publication of On the Origin of Species, nor were they bad observers before that date. And keep in mind a related point: religious commitment had little to do with the sorts of conclusions natural historians and biologists reached before Darwin, and it seems that in science, it still does not now.

The evolution of the species conceptThen God said, Let the land produce vegetation: seed-bearing plants and trees on the land that bear fruit with seed in it, according to their various kinds. And it was so. The land produced vegetation: plants bearing seed according to their kinds and trees bearing fruit with seed in it according to their kinds. And God saw that it was good. …

And God said, Let the water teem with living creatures, and let birds fly above the earth across the expanse of the sky. So God created the great creatures of the sea and every living and moving thing with which the water teems, according to their kinds, and every winged bird according to its kind. And God saw that it was good. …

And God said, Let the land produce living creatures according to their kinds: livestock, creatures that move along the ground, and wild animals, each according to its kind. And it was so. God made the wild animals according to their kinds, the livestock according to their kinds, and all the creatures that move along the ground according to their kinds. And God saw that it was good.

Genesis 1, verses 11–2, 20–1, 24–5, New International Version

So long as people have been farming plants and raising livestock, they have been aware that one organism gives birth to another very like it. That is, they have known that living things come in kinds. This is not confined to the Bible, of course. Aristotle knew it. So did Theophrastus, his student, sometimes called the father of botany. It is not, as they say, rocket surgery.

So given the relatively short time scale of human observation, it followed that people would tend to think that species, living kinds, were stable; and they did. But they did not think species were unable to change for a very long time, not until John Ray, a brilliant English 17th-century botanist who compiled the first complete flora (of Cambridgeshire, and then of England), wrote in an influential work:

After long and considerable investigation, no surer criterion for determining species has occurred to me than the distinguishing features that perpetuate themselves in propagation from seed. Thus, no matter what variations occur in the individuals or the species, if they spring from the seed of one and the same plant, they are accidental variations and not such as to distinguish a species … Animals likewise that differ specifically preserve their distinct species permanently; one species never springs from the seed of another nor vice versa.

This was the first recorded biological definition of "species", although the logical term had been used in biological contexts for a long time prior to that. But his was not the traditional view. Following a suggestion of Aristotle that new species were formed by hybridization at water holes in Africa, St Augustine, among others (including one of the translators of the King James Bible), happily accepted that new species could be formed out of old ones. Linnaeus himself, who is sometimes regarded as the originator of species fixism, observed hybridization between two plant species in his own garden, and late in life revised his view that species were as the "Infinite Being" had first created them. Certainly there was no tradition in Christian theological circles that species had to be unchanging before then.

During the Middle Ages, little natural history — or biology as we would now call it — was being done. But there was an exception: the Holy Roman Emperor Frederick II of Hohenstaufen (1194–1250) was a keen falconer, and wrote, literally, the book on it, finding that Aristotle was sometimes a bit too credulous, and worse that he failed to discuss hawks, falcons, and hunting birds. Frederick had the resources and the time to do a proper study, and he found that bird species were not simple things at all. He settled on interbreeding as a standard. Albert the Great, who had access both to Frederick's falconers and writings, followed this idea. But both still took seriously enough the old idea of spontaneous generation of species from other species to investigate it. Frederick sent envoys to Sweden looking for evidence for or against the idea that the barnacle goose arose out of worms (which is how it got its name). He found no evidence and concluded that the idea was based on ignorance. Albert did breeding experiments and managed to show that the geese laid eggs in the usual manner.

So we should first of all abandon the idea that people before Darwin thought that species were fixed, necessarily. Some did; many did not. Moreover, almost as soon as the idea of species-fixism caught on, it was challenged. Linnaeus made the idea popular in his Systema Naturae, the first edition of which was in 1735. In 1745, physicist Pierre Maupertuis argued in his Physical Venus that species did evolve, that they did so through a crude version of natural selection, and that inherited characteristics were passed on in a 3:1 ratio through both mother and father. While this did not influence many people at the time, it indicates that fixism was not universal among scientists even when it was still a new idea.

Why is it that we tend to think pre-Darwinians were all fixists? In part this is because Darwin has been used as a turning point in modern biology, which of course he was, and so some, the leading evolutionist Ernst Mayr among them, have tried to make him the ultimate source of all that is correct in modern biology. Furthermore, we think that religious belief before Darwin must have forced people to be fixists. But many quite orthodox Christians held to transmutation of species, and in some cases where this was denied, such as by the great anatomist Baron Cuvier, it was not for religious reasons but from a lack of evidence (although Cuvier managed to present the evidence that florae and fauna were not constant through time, even in Europe).

It is also not true that belief in creation as such forced a species-fixist position. Apart from deism, which perceived God as a creator who effectively left the world to run by the laws he created, many Christians held that the work of creation was still under way. And Christians who were natural historians, whether botanists or zoologists, often described species fairly well.

There is another myth — that before Darwin naturalists thought that species were defined by their morphology or their "essence". But morphology was used by taxonomists simply as a way to identify species, not as the cause of them, and even Linnaeus knew that his "Natural System", as it came to be called, was a useful convention, not a natural system at all. Taxonomists argued about how to define species, but in nearly all cases this was about how many and what kinds of characters were reliable. In the early 19th century, there was no "species problem", but only a "species question", which a minor geologist by the name of Charles Lyell called "that mystery of mysteries" — why were there species? It was not a question he, an orthodox Christian, thought could be answered from Scripture. Neither did his eventual disciple Darwin think that.

Darwin's view of species has likewise been misunderstood, in part because he did not really consider the definition of a species to be the primary question. Like many professional taxonomists (Darwin wrote the first and still one of the best descriptions of barnacles), he found the constant squabbling about whether this variety or that was a separate species or the same to be a nuisance to doing the work. He cited with wry amusement one taxonomist, Phillips, who declared "at last I have found out the only true definition — ‘any form which has ever had a specific name'!" And there was, in 1842, a set of standards from which all modern taxonomic rules derive — Darwin was a committee member — which formally instituted the rule of Linnaeus that species had to have a binomial (a genus and species name), and that only professionals could name species (to stop bird-watching enthusiasts naming every different plumage as a species). In the Origin, he wrote:

… it will be seen that I look at the term species as one arbitrarily given, for the sake of convenience, to a set of individuals closely resembling each other, and that it does not essentially differ from the term variety, which is given to less distinct and more fluctuating forms. The term variety, again, in comparison with mere individual differences, is also applied arbitrarily, for convenience's sake.

On the basis of this and other comments, he seemed to be saying that a species was not a real thing, but that it was just what we called something for convenience. But in his works overall, he treats species as real things, mostly (but not always) isolated by infertility, with different ecological adaptations. His point was, and it remains a sticking point today, that the difference between a species and a variety within a species was vague. This, of course, is due to the fact that species, like sand dunes, rivers and clouds, have no hard and sharp boundaries between them because of evolution.

About the time evolution had been universally accepted by naturalists (now called biologists), but before the new Darwinism of the synthesis of genetics and evolution had been settled, one EB Poulton wrote a paper in 1903 entitled "What is a species?" in which he addressed what now became the species "problem". This set the agenda for the next century. From being the useful identification of kinds that might vary, in the late Middle Ages and after, through to being a problem of who got to name species and how they were to be differentiated, now species were the "units" of evolution, and of biology in general. And a veritable explosion of attempts to define species followed. By the end of the 20th century, there had been some 22 distinct concepts identified by RL Mayden, and depending on how one divides them, some few others have been added. By my count, there are around 26 concepts (see sidebar, p 42–3).

Well, not exactly concepts. There is only one concept, which we label by the word "species". There are 26 or so conceptions, or definitions, which we define in other ways. This slightly picky philosophical point matters. We are arguing over the best way to define a concept. This depends on scientific data, theory, and other factors (some of them political, within the scientific community). We might deny that the concept even has a useful definition, or we might think that we have been misled by the use of a single word and seek a number of different concepts that serve the purposes of science and knowledge. I mention this because one of the oft-repeated claims made by anti-evolutionists is that if we cannot define our terms, we cannot show that species evolve. This canard goes back to Louis Agassiz, the famous geologist and paleontologist, who single-handedly introduced America to biology. Agassiz wrote:

If species do not exist at all, as the supporters of the transmutation theory maintain, how can they vary? And if individuals alone exist, how can differences which may be observed among them prove the variability of species?

Darwin rightly snorted to Agassiz's one-time student Asa Gray:

I am surprised that Agassiz did not succeed in writing something better. How absurd that logical quibble — "if species do not exist how can they vary?" As if anyone doubted their temporary existence.

Creationists will often claim that they are not interested in the species level, though. Initially, creationism did require fixity of species. In the 1920s, when George McCready Price equated "species" to the biblical "kinds", he was forced, to allow for the Ark to carry "every kind", to raise the bar higher. Even this was not original. In the late 18th century, Buffon, Cuvier's predecessor, had suggested that there was a "first stock" from which all members of a kind had evolved, so that all cats evolved from an original animal, modified by geography and climate, for instance. So creationists themselves have a "vagueness problem" no less than evolutionary biology does. Life is vague. Certainly the creationist "kind", or "baramin", as they mangle the Hebrew for "created kind", is extremely elastic. Given that elasticity, the motivation for the inference that was made naturally during the 17th and 18th centuries that species do not evolve is undercut. If kinds are not exact in reproduction, why think that the Genesis account is enough to prohibit evolution? The answer is, of course, that biblical literalism is not the primary motivation here for opposition to evolution.

The species problem

Reproductive isolation conceptionsIt begins in 1935, when a young fruit fly geneticist named Theodosius Dobzhansky published a paper "A critique of the species concept in biology" in a philosophy journal. Not that there had not been developments after Darwin. Various people had suggested that species were "pure gene lines" or "wild-types" that did not vary much. Mendelian genetics caused a lot of debate about species. Dobzhansky claimed that a species was:

… a group of individuals fully fertile inter se, but barred from interbreeding with other similar groups by its physiological properties (producing either incompatibility of parents, or sterility of the hybrid, or both).

This was the original genetic version of reproductive isolation concepts (Buffon had proposed interbreeding as a test a century and a half earlier, which Darwin rejected). Unfortunately, a version framed by Ernst Mayr got called the "biological" species concept, in contrast to what were seen as "nonbiological" concepts that relied largely on form and based in museum taxonomy, which were called "morphological" concepts by Mayr. But I think it is better to call these Reproductive Isolation Species Concepts (RISC) than "biological" ones, for any decent species conception is biological. Mayr's version changed over the years, but the one taught to most undergraduate biology students is the original:

A species consists of a group of populations which replace each other geographically or ecologically and of which the neighboring ones intergrade or interbreed wherever they are in contact or which are potentially capable of doing so (with one or more of the populations) in those cases where contact is prevented by geographical or ecological barriers.

Or shorter:

Species are groups of actually or potentially interbreeding natural populations, which are reproductively isolated from other such groups.

Much of the focus on species after this centered on Reproductive Isolating Mechanisms, or RIMs for short. Mayr's view was that species are formed when part of the species is geographically isolated from the main range and evolves in its own way such that when it gets back in contact, RIMs have evolved, as it were, by accident, and the two no longer interbreed successfully. Selection against hybrids, which are, so to speak, neither fish nor fowl in ecological adaptations, then strengthens the isolation (a process called "re-inforcing selection"). Mayr's version of the origin of species, published in 1942 and reiterated for the next 60 years (Mayr survived to 100, outliving many of his adversaries, and thus getting the last word), is called the allopatric theory of speciation. Allopatry means that two populations, or species, or groups, of organisms live in different areas (allo- = other, patria = homeland). The alternative kind of speciation, which is in effect Darwin's view, is called sympatric (sym- = together) speciation, and it is highly contentious among specialists, with some thinking that it occurs, particularly among fruitflies and lake-bound fishes, where it has been studied, and others thinking that it does not, and the debate goes on. It requires that RIMs evolve in place, so to speak, and the naysayers think this is unlikely to occur. If sympatric speciation does occur, then there can only be one reason — natural selection. Recent theoretical work shows that it is possible if the conditions are right. What we do not yet know for sure is how often the conditions are right.

There is another uncontested class of speciation processes — usually involving hybridization, that old idea of Aristotle. In plants particularly, but also in animals, fungi, bacteria, and so on, sometimes entire genetic complements can double, triple or more, resulting in a condition known as polyploidy. When this happens, sometimes the chromosomes and genes do not line up due to differing genetic structures of the parents, but an extra doubling of the genome, followed by a cell division, can give the cell a paired set of chromosomes, allowing it effectively to found a new species in one or a few generations. When two species interbreed, this allows the resulting organism to have a matched set of chromosomes. It has been estimated that nearly all ferns, for example, have a case of polyploidy in their ancestry, and as many as 7% of actual fern species are formed this way. It has also been seen in flowering plants, corals, grasshoppers, other insects, and reptiles. It is even hypothesized that the entire mammalian branch of the evolutionary tree was started with this kind of event. So in a sense, Linnaeus and Aristotle were right … sort of. Even Mendel thought this might be the reason why new species evolve, which informed his research into hybrid forms, although he studied hybridization within, not between, species.

Evolutionary conceptionsSo the RISC conceptions have a lot of leeway for interpretation. But they are not the only conceptions on the board. One kind of conception goes by the name evolutionary species concepts, which is also a misnomer (because all species have evolved). On this view, it does not much matter if two possible species under consideration are reproductively isolated. Even if there is gene flow between them on a regular basis, what counts is whether or not they remain evolutionarily distinct. Dobzhansky's definition has a hint of this, but the original formulation is due to a paleontologist, George Gaylord Simpson. Simpson defined it this way in 1961, although there is an earlier and more technical definition from ten years before:

An evolutionary species is a lineage (an ancestral–descendant sequence of populations) evolving separately from others and with its own unitary evolutionary role and tendencies.

What counts here is that no matter what happens in terms of gene exchange, the populations remain distinct, and have their own forms, adaptations, and fate. The term "lineage" used here is particularly important, as it focused biologists' thinking more in evolutionary terms, and gave rise to yet another class of conceptions — phylogenetic species concepts.

Evolutionary conceptions have been expanded since Simpson to include asexual organisms (which do not, strictly speaking, form populations, since that term involves interbreeding). The important point is that there is a single lineage over time. In contrast, the RISC conceptions involve a single time "horizon", which means that a species is something that at a particular time and place is not interbreeding with other populations, and they also, necessarily, exclude asexual organisms.

Phylogenetic conceptionsThere is a group of species conceptions that go under the shared name of phylogenetic species concepts. A phylogeny is, of course, an evolutionary history, and the initial proposal for a phylogenetic conception came from Willi Hennig, an East German entomologist who nevertheless managed to influence a great many biologists during the height of the Cold War. Hennig's methodology and philosophy of classification is known today as "cladistics".

Hennig did not set out to come up with a new species concept. He pretty much assumed something like an amalgam of Mayr's and Simpson's definitions. The difference was that he focused on the lineage element, and combined it with a clear and formal account of making groups logically. In his book Phylogenetic Systematics, translated into English in 1966, he included a diagram about speciation (redrawn above as Figure 1), and when to name a new species.

There are several lineages in this diagram. Ignoring the technical terminology (Hennig was a great one for coining classical names), you can see that each individual organism is part of a genealogical lineage. These, when grouped together, form a species lineage. Clearly what makes a species lineage is the fact that the overall tangled net of genealogical lineages has not yet divided (as in the right-hand diagram marked "phylogenetic relationships"). When it has, says Hennig, the old species is extinguished and two new ones come into being (as in the separate circles at the top).

This provision caused a lot of anxiety. It seemed to be saying that a species has to go extinct when new ones come into being, but of course a new species can evolve without modifying the old one much, if at all. Hennig's convention, as it is known, was more a point about naming species than a definition of their biological nature. When a new species arises, the old name refers to only a part of its descendants and for Hennig that meant it was no longer a "natural" group being named. It is rather like calling rock music "blues" because it is a descendant of blues. What Hennig said would mean that what is still "blues" has to get a new name so that musicologists can talk without ambiguity (so it might get called "traditional blues").

I'm extremely aware of all that. I studied that stuff for years. I taught it! It should be mentioned, though, that species is not at all the same as the biblical 'kind.' The 'kind' would be much more akin to a family or sub-family in our current taxonomic classification system. Equine, bovine, feline, canine, etc.

I don't know anyone who is at all versed in the argument between evolution and creation trying to equate kind with species, unless it is being used as some kind of red herring argument by evolutionists.

No matter what I post you are going to pooh-pooh it, because you have made up your mind that Evolution is wrong.So, I thought I would give you something to read and think about.

Victor,

Helen can answer for herself, she more than capable of doing so, but I will say this: Your article that you chose to post said: "a virtue of biology" Your accept by your wisdom that biology apart form the testimony of scripture has more virtue than the truth of God's word?

Paul called biology~science falsely so called! All teachings must be brought back to the bible in order to have any support of truthfulness and specially that most sacred word: VIRTUE!

I do not waste much time with fools, who reject God's testimony over and above the wisdom of man.

Apart from the most rabid fundamentalists among us, nearly everyone admits that the Bible might contain errors -- a faulty creation story here, a historical mistake there, a contradiction or two in some other place. But is it possible that the problem is worse than that -- that the Bible actually contains lies?

Most people wouldn't put it that way, since the Bible is, after all, sacred Scripture for millions on our planet. But good Christian scholars of the Bible, including the top Protestant and Catholic scholars of America, will tell you that the Bible is full of lies, even if they refuse to use the term. And here is the truth: Many of the books of the New Testament were written by people who lied about their identity, claiming to be a famous apostle -- Peter, Paul or James -- knowing full well they were someone else. In modern parlance, that is a lie, and a book written by someone who lies about his identity is a forgery.

Most modern scholars of the Bible shy away from these terms, and for understandable reasons, some having to do with their clientele. Teaching in Christian seminaries, or to largely Christian undergraduate populations, who wants to denigrate the cherished texts of Scripture by calling them forgeries built on lies? And so scholars use a different term for this phenomenon and call such books "pseudepigrapha."

I have never made it a secret that I am an agnostic and I usually only post in response to negative attacks on Evolution, but Red Baker went too far.

Victor, do not get so upset, God uses the word fools many times in reference to those who say that there is no God. Every person living has at one time or another including myself show that we are fools, when we depart from the wisdom of the scriptures. So, only those who consider themselves wise, above the scriptures would be upset at such a statment.

Psalm 14:1

"The fool hath said in his heart, There is no God. They are corrupt, they have done abominable works, there is none that doeth good."

There are many, many more dealing with fools. Do not get upset at me~maybe at yourself, for rejecting the: VIRTUE of the truth of the holy scriptures, for the blabblings by men who think that they are wise.